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Symbiotic plant peptides eliminate Candida albicans both in vitro and in an epithelial infection model and inhibit the proliferation of immortalized human cells.

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Tartalom: http://real.mtak.hu/28481/
Archívum: MTA Könyvtár
Gyűjtemény: Status = Published

Type = Article
Cím:
Symbiotic plant peptides eliminate Candida albicans both in vitro and in an epithelial infection model and inhibit the proliferation of immortalized human cells.
Létrehozó:
Ordögh, Lilla
Vörös, Andrea
Nagy, István
Kondorosi, Eva
Kereszt, Attila
Dátum:
2014
Téma:
QR180 Immunology / immunológia
Tartalmi leírás:
The increasing number of multidrug-resistant microbes now emerging necessitates the identification of novel antimicrobial agents. Plants produce a great variety of antimicrobial peptides including hundreds of small, nodule-specific cysteine-rich NCR peptides that, in the legume Medicago truncatula, govern the differentiation of endosymbiotic nitrogen fixing bacteria and, in vitro, can display potent antibacterial activities. In this study, the potential candidacidal activity of 19 NCR peptides was investigated. Cationic NCR peptides having an isoelectric point above 9 were efficient in killing Candida albicans, one of the most common fungal pathogens of humans. None of the tested NCR peptides were toxic for immortalized human epithelial cells at concentrations that effectively killed the fungus; however, at higher concentrations, some of them inhibited the division of the cells. Furthermore, the cationic peptides successfully inhibited C. albicans induced human epithelial cell death in an in vitro coculture model. These results highlight the therapeutic potential of cationic NCR peptides in the treatment of candidiasis.
Típus:
Article
PeerReviewed
info:eu-repo/semantics/article
Formátum:
text
Azonosító:
Ordögh, Lilla and Vörös, Andrea and Nagy, István and Kondorosi, Eva and Kereszt, Attila (2014) Symbiotic plant peptides eliminate Candida albicans both in vitro and in an epithelial infection model and inhibit the proliferation of immortalized human cells. BioMed research international, 2014. p. 320796. ISSN 2314-6141
Kapcsolat:
269067